Obadia J F, Ben Baouali A, Maupoil V, Rochette L
Service de Chirurgie Cardiothoracique et vasculaire, Höpital Cardiologique Louis-Pradel, Hospices Civils de Lyon, BP Lyon-Montchat.
Ann Chir. 1996;50(5):390-6.
Post-ischemic reperfusion phenomena were studied in two methods of myocardial protection: crystalloid cardioplegia (St Thomas n(o) 2) and cold blood cardioplegia (Buckherg) during cardiopulmonary bypass for human myocardial revascularisation. Myocardial protection was assessed on the course of hemodynamic parameters, reperfusion arrhythmias and biochemical analysis of the coronary flow after cross-clamp removal: creatine phosphokinase (CPK-MB) and nucleotide adenine metabolites (adenosine, inosine, hypoxanthine, xanthine and uric acid). The study was performed in two groups of 14 patients. Hemodynamic conditions were similar in both groups during reperfusion in order to avoid different coronary flow. Under these conditions, myocardial protection by cold blood cardioplegia reduced reperfusion arrhythmias, and resulted in a loss of CPK-MB release. Furthermore, cold blood cardioplegia provided protection of myocardial energy metabolism by reducing the loss of metabolites, purine bases and oxypurine bases into the coronary sinus. Our results also show that hypoxanthine is probably the final product of ATP degradation in human myocardial tissue.
在人体心肌血运重建的体外循环过程中，采用两种心肌保护方法研究了缺血后再灌注现象：晶体停搏液（St Thomas no. 2）和冷血停搏液（Buckherg）。通过血流动力学参数变化过程、再灌注心律失常以及松开主动脉阻断钳后冠状动脉血流的生化分析（肌酸磷酸激酶（CPK-MB）和核苷酸腺嘌呤代谢产物（腺苷、肌苷、次黄嘌呤、黄嘌呤和尿酸））来评估心肌保护效果。该研究在两组各14例患者中进行。为避免冠状动脉血流不同，两组在再灌注期间的血流动力学状况相似。在这些条件下，冷血停搏液的心肌保护作用减少了再灌注心律失常，并导致CPK-MB释放量减少。此外，冷血停搏液通过减少代谢产物、嘌呤碱和氧嘌呤碱进入冠状窦，对心肌能量代谢起到了保护作用。我们的研究结果还表明，次黄嘌呤可能是人体心肌组织中ATP降解的最终产物。
